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Alencar, Dentistry 2013, 3:2

Volume 3 Issue 2 1000e112
ISSN: 2161-1122 Dentistry, an open access journal
Open Access Editorial
Chronic Orofacial Pain, Central Sensitization and Sleep Is There a Link?
Francisco Alencar Jr*
General Dental Sciences Department, TMD and Orofacial Pain, Marquette University School of Dentistry, Milwaukee, WI, USA
*Corresponding author: Francisco Alencar Jr. DDS, MS, MS, PhD, General
Dental Sciences Department, TMD and Orofacial Pain, Marquette University School of
Dentistry, Milwaukee, WI, USA, Tel: 414-288-5590; E-mail: docfalencarjr@yahoo.com,
Received November 04, 2013; Accepted November 06, 2013; Published
November 08, 2013
Citation: Alencar F (2013) Chronic Orofacial Pain, Central Sensitization and
Sleep Is There a Link? Dentistry 3: e112. doi:10.4172/2161-1122.1000e112
Copyright: 2013 Alencar F. This is an open-access article distributed under the
terms of the Creative Commons Attribution License, which permits unrestricted
use, distribution, and reproduction in any medium, provided the original author and
source are credited.
Pain has been cited in very ancient texts such as the Old and New
Testament in the Bible. However, it was only defned in the scientifc
literature in 1986 when the International Association for the Study
of Pain (IASP) provided ofcially their frst classifcation and pain
description [1].
Contrary to what one might think, pain cannot be defned only
as an unpleasant sensation. Pain is a highly subjective experience that
involves the peripheral and central nervous system and is infuenced
by previous experiences, emotional and cognitive factors. It has
long been appreciated that the experience of pain is highly variable
between individuals. Pain results from activation of sensory receptors
specialized to detect actual or impending tissue damage (nociceptors).
Nevertheless, a direct correlation between activation of nociceptors
and the sensory experience of pain is not always apparent. Even in
cases in which the severity of injury appears similar, individual pain
experiences may vary dramatically. Emotional state, degree of anxiety,
attention and distraction, past experiences, memories, and many other
factorscan either enhance or diminish the pain experience. Tis is what
we call pain modulation [2].
Pain could also be viewed as a protective or defensive mechanism
that sends the brain an alert so a protective behavior can be generated.
Nevertheless in Chronic Pain this purpose is missing. When pain lasts
longer than it is supposed afer healing has happened, it can in fact turn
to be an etiologic factor. Terefore pain cannot be viewed only as a sign
or a symptom of a disease. Tis fnding has a profound impact in the
way Chronic Pain should be viewed by health care providers. Also it
should create a shif in patients behavior towards pain management.
In other words, this means that treating pain is not only palliative or
supportive care. When managing pain properly we are in fact treating
or controlling a potential or actual etiologic factor. Pain can cause
transient or irreversible changes in the peripheral and central nervous
system, clinically resulting in Myofascial Pain, Neuropathic Pain and
other complex pain syndromes.
Tere has been an extensive debate towards the length or duration
of pain to be considered chronic. Usually 3 months or 6 months would
be considered the minimal pain duration. Te question is: Why is
it important to diferentiate between chronic and acute pain? Te
importance relies in the need to treat these patients with a diferent
approach. Te diference is usually related to the presence of Central
Sensitization, Sleep Dysfunction and severe Psychological Issues.
Terefore the debate about time/duration becomes of a secondary
importance since the presence of signs or symptoms of Central
Sensitization and Poor Sleep quality becomes the key topics in Chronic
Pain defnition and consequently management.
In order to understand Central Sensitization we need to consider
pain not as a sign or symptom of a disease or pathological disorder.
We need to see pain with a potential to cause damage to the Central
Nervous System (CNS) according to its severity, intensity and duration.
In other words, the longer the duration and the greater the pain
intensity, chances are that some sort of damage will occur in the CNS.
Central sensitization represents an enhancement in the function of
neurons and circuits in nociceptive pathways caused by increases in
membrane excitability and synaptic efcacy. Te whole CNS becomes
oversensitive and will respond not only to painful stimulations, but
rather to all sorts of excitations in a very diferent and peculiar way.
Tis change may afect diferent autonomic, sensory and motor fbers.
When afecting autonomic fbers the patient can clinically manifest
signs and symptoms that will resemble an allergic or sinus infection.
Tese could be facial swelling, increase in skin temperature, redness,
eye lacrimation, rhinorrhea, nasal congestion, sneeze and cough
among others. Sensory or sensitive fbers may be afected and present
clinically as allodynea or secondary hyperalgesia. Motor fbers can
initially present muscle protective co-contraction that if postergated
will originate muscle myalgia and perhaps myofascial pain. Interesting
to note is that all these diferent clinical presentations are constantly
misdiagnosed and they are all caused by constant pain input.
It is not surprising that patients with chronic headaches have a
higher prevalence of myofascial trigger points, and headache symptoms
that can be reproduced by stimulation of an active trigger point [3].
Trough my research I have found that the presence of trigger points
may be a contributing factor in the initiation and/or perpetuation of
chronic headaches. Myofascial pain can be the cause, along with the
evidence of central sensitization, of atypical facial pain, with trigger
points referring pain to the teeth, gums, maxillary sinus, mandible,
ears, face, head and /or some kind of vision impairment [4].
When a referred patient presents for an emergency consult
indicating tooth pain, he could actually be sufering from Myofascial
Pain Disorder (MPD.) All practitioners who treat pain patients,
especially chronic pain patients, need to study and better understand the
etiology in order to come out with an adequate diagnosis. Considering
only occlusion or psychological issues as potential etiologic factors to
TMD or MPD is not considered evidence based Dentistry.
Patients have undergone invasive surgery procedures, including
teeth extractions and TMJ surgery, when the diagnosis was myofascial
pain or neuropathic pain. Neuropathic pain etiology used to be linked
only when some nerve damage had occurred. In fact this can be one
of the causes of neuropathic pain, but inadequately managed chronic
pain can lead to central sensitization and neuropathic pain as well. Tis
can be caused due to changes in the peripheral and central nervous
system. It can be even more confusing because it is usually described
as a burning, electrical shock like or throbbing pain. If this pain is
being felt in some teeth or head, can be easily confused and diagnosed
as odontogenic pain or migraine.
Evidence based Dentistry points in one direction for the management
of Chronic TMD and other Orofacial Pain conditions. It is now known
Volume 3 Issue 2 1000e112
ISSN: 2161-1122 Dentistry, an open access journal
Citation: Alencar F (2013) Chronic Orofacial Pain, Central Sensitization and Sleep Is There a Link? Dentistry 3: e112. doi:10.4172/2161-
Page 2 of 2
that a combination of many factors contribute to this condition.
Sleep quality, daytime posture, habits including work environment,
posture during sleep, insufcient hydration, cafeine intake, nicotine
intake, daytime parafunctions and sleep bruxism, anxiety, frustration
and depression, can all afect the Central Nerve System (CNS) and
cause more pain or perpetuate the pain through central sensitization.
Inadequate occlusion could be a consequence and not the cause of
infammation in the temporomandibular joint. In multiple cases with
TMD and/or TMJ infammation the patient completed treatment with
a much better an adequate occlusal relationship.
Chronically painful conditions are frequently associated with sleep
disturbances, i.e. changes in sleep continuity and sleep architecture
as well as increased sleepiness during daytime. A new hypothesis,
which has attracted more and more attention, is that disturbances
of sleep cause or modulate acute and chronic pain. Since it is well-
known that pain disturbs sleep, the relationship between the two has
since recently been seen as reciprocal. According to the majority of the
studies, sleep deprivation produces hyperalgesic changes. Furthermore,
sleep deprivation can interfere with analgesic treatments involving
opioidergic and serotoninergic mechanisms of action [5]. Tis is very
important information that clinicians dealing with chronic pain should
never forget.
Laboratory based sleep deprivation studies have also suggested that
reductions in total sleep time are accompanied by increased sensitivity
to noxious stimuli (secondary hyperalgesia) and by decrements in
endogenous pain-inhibitory processes. Tis could also be a link
between chronic pain and central sensitization (CS), since secondary
hyperalgesia and other secondary excitatory efects specifcally related
to CS could be related to a longer duration of the pain causing a
reduction of the sleep time. Alternatively, a relatively long sleep period
may indicate poor sleep continuity (e.g., fragmented, or overly light
sleep), which has been associated with enhanced pain perception in
some laboratory studies of experimental sleep fragmentation [6].
It is a very complex area due to the numbers of factors that can
be involved, the need for the clinician to study other areas not related
directly with Dentistry and the controversies in the literature most
of the times caused by grouping a lot of diferent subtypes of TMD
diagnosis in one big group and call it TMD.
It seems to be clear and evident that sleep and pain have a close
relationship. Also, chronic pain can cause sleep disturbances and
central sensitization. Health care providers who treat patients in pain
must be familiar with these concepts as well as treatment modalities to
manage them.
1. Mersky H (1986) Classifcation of chronic pain: Description of chronic pain
syndromes and defnition of pain terms. Pain 3: S1-226.
2. Ossipov MH, Dussor GO, Porreca F (2010) Central Modulation of Pain. J Clin
Invest 120: 3779-3787.
3. Sanit PV, Alencar Jr FGP (2009) Myofascial Pain Syndrome as a contributing
factor in patients with chronic headaches. Journal of Musculoskeletal Pain 17:
4. Alencar Jr FGP (2010) The Puzzling Problems of Myofascial Pain. Marquette
University Discover Magazine.
5. Lautenbacher S, Kundermann B, Jrgen-Christian Krieg (2006) Sleep
deprivation and pain perception. Sleep Medicine Reviews 10: 357-369.
6. Everson CA, Szabo A (2009) Recurrent restriction of sleep and inadequate
recuperation induce both adaptive changes and pathological outcomes. Am J
Physiol Regul Integr Comp Physiol 297: 1430-1440.
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Citation: Alencar F (2013) Chronic Orofacial Pain, Central Sensitization and
Sleep Is There a Link? Dentistry 3: e112. doi:10.4172/2161-1122.1000e112

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